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2017 ; 6
(7
): R131-R145
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English Wikipedia
Update on angiotensin II: new endocrine connections between the brain, adrenal
glands and the cardiovascular system
#MMPMID28855243
Leenen FHH
; Blaustein MP
; Hamlyn JM
Endocr Connect
2017[Oct]; 6
(7
): R131-R145
PMID28855243
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In the brain, angiotensinergic pathways play a major role in chronic regulation
of cardiovascular and electrolyte homeostasis. Increases in plasma angiotensin II
(Ang II), aldosterone, [Na(+)] and cytokines can directly activate these
pathways. Chronically, these stimuli also activate a slow neuromodulatory pathway
involving local aldosterone, mineralocorticoid receptors (MRs), epithelial sodium
channels and endogenous ouabain (EO). This pathway increases AT(1)R and NADPH
oxidase subunits and maintains/further increases the activity of angiotensinergic
pathways. These brain pathways not only increase the setpoint of sympathetic
activity per se, but also enhance its effectiveness by increasing plasma EO and
EO-dependent reprogramming of arterial and cardiac function. Blockade of any step
in this slow pathway or of AT(1)R prevents Ang II-, aldosterone- or salt and
renal injury-induced forms of hypertension. MR/AT(1)R activation in the CNS also
contributes to the activation of sympathetic activity, the circulatory and
cardiac RAAS and increase in circulating cytokines in HF post MI. Chronic central
infusion of an aldosterone synthase inhibitor, MR blocker or AT(1)R blocker
prevents a major part of the structural remodeling of the heart and the decrease
in LV function post MI, indicating that MR activation in the CNS post MI depends
on aldosterone, locally produced in the CNS. Thus, Ang II, aldosterone and EO are
not simply circulating hormones that act on the CNS but rather they are also
paracrine neurohormones, locally produced in the CNS, that exert powerful effects
in key CNS pathways involved in the long-term control of sympathetic and
neuro-endocrine function and cardiovascular homeostasis.
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